Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Jan:78:100-6.
doi: 10.1016/j.yjmcc.2014.09.023. Epub 2014 Sep 28.

The mitochondrial permeability transition pore: molecular nature and role as a target in cardioprotection

Paolo Bernardi  1 , Fabio Di Lisa  2
Affiliations
Review

The mitochondrial permeability transition pore: molecular nature and role as a target in cardioprotection

Paolo Bernardi et al. J Mol Cell Cardiol. 2015 Jan.

Abstract

The mitochondrial permeability transition (PT) - an abrupt increase permeability of the inner membrane to solutes - is a causative event in ischemia-reperfusion injury of the heart, and the focus of intense research in cardioprotection. The PT is due to opening of the PT pore (PTP), a high conductance channel that is critically regulated by a variety of pathophysiological effectors. Very recent work indicates that the PTP forms from the F-ATP synthase, which would switch from an energy-conserving to an energy-dissipating device. This review provides an update on the current debate on how this transition is achieved, and on the PTP as a target for therapeutic intervention. This article is part of a Special Issue entitled "Mitochondria: from basic mitochondrial biology to cardiovascular disease".

Keywords: Ischemia–reperfusion injury; Mitochondria; Permeability transition pore.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Raaflaub J. Die schwellung isolierter leberzell mitochondrien und ihre physikalisch beeinfluβarkeit. Helv Physiol Pharmacol Acta. 1953;11:142–156. - PubMed
    1. Raaflaub J. Über den wirkungsmechanismus von adenosintriphosphat (ATP) als cofaktor isolierter mitochondrien. Helv Physiol Pharmacol Acta. 1953;11:157–165. - PubMed
    1. Hunter F.E., Jr., Ford L. Inactivation of oxidative and phosphorylative systems in mitochondria by preincubation with phosphate and other ions. J Biol Chem. 1955;216:357–369. - PubMed
    1. Tapley D.F. The effect of thyroxine and other substances on the swelling of isolated rat liver mitochondria. J Biol Chem. 1956;222:325–339. - PubMed
    1. Lehninger A.L., Remmert L.F. An endogenous uncoupling and swelling agent in liver mitochondria and its enzymic function. J Biol Chem. 1959;234:2459–2464. - PubMed

Publication types

MeSH terms

Substances